带有集成诱的受体对将致病原体的转录因子禁用转化为免疫
Clémentine Le Roux1, Gaëlle Huet2, Alain Jauneau3
1INRA, Laboratoire des Interactions Plantes-Microorganismes (LIPM), UMR441, Castanet-Tolosan 31326, France; CNRS, Laboratoire des Interactions Plantes-Microorganismes (LIPM), UMR2594, Castanet-Tolosan 31326, France; Department of Plant-Microbe Interactions, Max Planck Institute for Plant Breeding Research, Carl-von-Linne-Weg 10, Köln 50829, Germany.
Cell
|May 23, 2015
概括
植物免疫受体 (NLR) 检测出细菌效应体. 我们发现一种细菌效应剂可乙化植物免疫受体 (RRS1-R),破坏其DNA结合并触发免疫力.
科学领域:
- 植物免疫力 植物免疫力
- 分子植物病原体相互作用
- 微生物毒性机制是微生物毒性机制.
背景情况:
- 植物细胞内核酸结合/氨酸丰富的重复受体 (NLRs) 检测病原体因子,触发防御.
- RRS1-R和RPS4 NLR对赋予了对Ralstonia solanacearum的耐药性,从而提供了PopP2效应器.
研究的目的:
- 阐明RRS1-R和RPS4对PopP2.2产生抗性的机制.
- 了解细菌效应器如何操纵植物防御通路.
主要方法:
- 生物化学测试以检测效应器触发的乙化.
- 对转录因子DNA结合活性的分析.
- 评估植物的免疫反应和抗病能力.
主要成果:
- 乙转移酶效应剂PopP2直接在RS1-R免疫受体上乙化 lysine 残留物.
- 乙化破坏了RRS1-R的WRKY域的DNA结合能力.
- 这种乙化事件触发了依赖RPS4的植物免疫力.
- PopP2通过乙化向多个促进防御的 WRKY 转录因子,损害它们的 DNA 结合和功能.
结论:
- RRS1-R NLR集成了效应器检测与DNA关联来激活免疫力.
- 细菌病原体可以重新利用宿主乙化机制来抑制植物的防御.
- 这项研究揭示了一种新的策略,即细菌效应器将其毒性活动转换为防御基因激活.
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